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Table 10 Impact of resveratrol on the expression of genes in the context of other cancers

From: Disease-associated regulation of gene expression by resveratrol: Special focus on the PI3K/AKT signaling pathway

Type of cancer

Dose range

Cell line

Target

Pathway

Function

Refs.

In vivo studies

Breast cancer (BCa)

50 mg/kg, 10–200 mg/L

MCF-7/DOX, MCF-7, MDA-MB-231

Caspase-3, P70S6K

PI3K/AKT/mTOR

RVT via inhibiting PI3K/AKT/ mTOR pathway could play a role in DOX resistance in breast neoplasm

[90]

Papillary Thyroid cancer (PTC)

30 mg/kg 50 μM

KTC-1,TPC-1

Caspase-3/8/9, Bax, Bcl-xl, Mcl-1, p70S6K

PI3K/AKT/mTOR

RVT via the PI3K/AKT/mTOR pathway could promote the anti-tumor effects of rapamycin in papillary thyroid cancer

[89]

Glioblastoma multiforme (GBM)

10 mg/kg, 0–20 μM

GICs

IKKα/β, JNK, mTOR, ERK1/2, IκBα p38, MMP-2, Lamin-A, Nestin, GFAP

PI3K/ AKT/NF-κB

RVT via downregulating PI3K/AKT/NF-κB pathway could inhibit invasion of glioblastoma-initiating cells (GICs)

[91]

In vitro studies

Melanoma

4 μM-18 μM

Human melanoma cell

–

AKT

RVT via dephosphorylation of AKT could overcome resistance to vemurafenib in BRAF-mutated melanoma cells

[86]

Melanoma

100 μM

B16

LC3-l, LC3-ll, Beclin-1, S6K, 4E-BP1

Ceramide/AKT/mTOR

RVT via the ceramide/AKT/mTOR pathway could trigger protective autophagy in melanoma B16 cells

[87]

Melanoma

0–100 μM

B16-F10, A375

Beclin-1, Caspase-9, P62, LC3II/I

PI3K/ AKT/mTOR

RVT via inhibiting the PI3K/AKT/mTOR pathway could promote autophagy and suppress melanoma growth

[92]

Pheochromocytoma

10–1000 μM

PC12

Caspase-3, iNOS

PI3K, AKT/p38 MAPK

RVT via AKT/p38 MAPK signaling could attenuate apoptosis, and protect neuronal cells from isoflurane-induced inflammation

[93]

BCa

10–25 μM

SK-BR-3, MCF7, T47D, MDA-MB-231

Caspase-7/8, JNK, P38, XIAP, Survivin, Bcl-2

AKT, HER-2, MAPK

RVT via inhibiting docetaxel-mediated activation of the HER-2/AKT axis could sensitize BCa cells to docetaxel-induced cytotoxicity

[88]

Bladder cancer

0–50 μmol/L

T24, 5637, SV-HUC-1

miR-21, Bcl-2, Caspase-3

AKT

RVT via miR-21 regulation of the AKT/Bcl-2 pathway could induce apoptosis of bladder cancer cells

[94]

Chondrosarcoma

25–100 μM

JJ012, SW1353

MMP2, MMP9

PI3K/AKT/MAPK

RVT via regulating the PI3K/AKT/MAPK pathway could inhibit cell proliferation and induce cell apoptosis in chondrosarcoma cells

[95]

Renal cell carcinoma (RCC)

0–100 μM

ACHN, A498, HK-2

N-cadherin, Vimentin, Snail, MMP-2/9, E-cadherin, TIMP-1

AKT, ERK1/2

RVT via inactivating the AKT and ERK1/2 pathways could inhibit proliferation and migration in RCC cells

[96]

Oral cancer

50 μM

CAR, CAL 27

LC3-II/I, Caspase-3/9, Atg-5/7/12/14, Beclin-1, Atg16L1, Apaf-1, AIF, Bcl-2, Bax, Bad

AKT/mTOR, AMPK

RVT via the AMPK and AKT/mTOR pathway could regulate autophagy and apoptosis in cisplatin-resistant human oral cancer CAR cells

[97]

Neuroblastoma (NB)

10–100 μM

SK-N-SH, SH-SY5Y, SK-N-Be2, SMS-KCNR, NB1691

GSK3β, IRS-1, Survivin, PP1α, α-tubulin

AKT

RVT via inactivating AKT by increasing PP1α activity could potentiate 2-DG-induced ER stress and NB cell death

[98]